It helped tumor cells to exacerbate glutamine deficiency in the microenvironment.[66, 70] Mechanistically, KRAS mutations upregulated the expression of glutaminase, which promoted enzymatic conversion of glutamine to downstream products.[71] Additionally, KRAS mutations increased the expression of aspartate transporters to facilitate the transport of mitochondrial glutamine‐derived aspartate into the cytosol. The gene discussed is KRAS; the disease is neoplasm.